TAp73 contributes to the oxidative stress response by regulating protein synthesis

Marini, A. et al. (2018) TAp73 contributes to the oxidative stress response by regulating protein synthesis. Proceedings of the National Academy of Sciences of the United States of America, 115(24), pp. 6219-6224. (doi: 10.1073/pnas.1718531115) (PMID:29844156) (PMCID:PMC6004440)

Abstract

Oxidative stress is a critical contributor to aging-associated diseases, including neurodegeneration, cancer, and cardiovascular disease. Here, we demonstrate that the p53 family transcription factor TAp73 contributes to the oxidative stress response by participating in the control of protein synthesis. Regulation of mRNA translation ensures a prompt and efficient method to overcome stress, and TAp73 depletion results in aberrant ribosomal biogenesis and impaired protein synthesis. In particular, TAp73 is important for maintaining active translation of mitochondrial transcripts in response to oxidative stress, thus promoting mitochondrial activity that contributes to adaptation to stress conditions. Our data therefore reveal an unexpected role for TAp73 in regulating protein synthesis responsible for its homeostatic ability.

• Item Type: Articles
• Status: Published
• Refereed: Yes
• Glasgow Author(s) Enlighten ID: Bushell, Professor Martin
• Authors: Marini, A., Rotblat, B., Sbarrato, T., Niklison-Chirou, M. V., Knight, J. R. P., Dudek, K., Jones, C., Bushell, M., Knight, R. A., Amelio, I., Willis, A. E., and Melino, G.
• College/School: College of Medical Veterinary and Life Sciences > School of Cancer Sciences
• Journal Name: Proceedings of the National Academy of Sciences of the United States of America
• Publisher: National Academy of Sciences
• ISSN: 0027-8424
• ISSN (Online): 1091-6490
• Published Online: 29 May 2018
• Copyright Holders: Copyright © 2018 The Authors
• First Published: First published in PNAS 115(24):6219-6224
• Publisher Policy: Reproduced under a Creative Commons License